Network analysis of online bidding activity

With the advent of digital media, people are increasingly resorting to online channels for commercial transactions. Online auction is a prototypical example. In such online transactions, the pattern of bidding activity is more complex than traditional online transactions; this is because the number of bidders participating in a given transaction is not bounded and the bidders can also easily respond to the bidding instantaneously. By using the recently developed network theory, we study the interaction patterns between bidders (items) who (that) are connected when they bid for the same item (if the item is bid by the same bidder). The resulting network is analyzed by using the hierarchical clustering algorithm, which is used for clustering analysis for expression data from DNA microarrays. A dendrogram is constructed for the item subcategories; this dendrogram is compared with a traditional classification scheme. The implication of the difference between the two is discussed.Comment: 8 pages and 11 figure

Continuous time dynamics of the Thermal Minority Game

We study the continuous time dynamics of the Thermal Minority Game. We find that the dynamical equations of the model reduce to a set of stochastic differential equations for an interacting disordered system with non-trivial random diffusion. This is the simplest microscopic description which accounts for all the features of the system. Within this framework, we study the phase structure of the model and find that its macroscopic properties strongly depend on the initial conditions.Comment: 4 pages, 4 figure

Strategy updating rules and strategy distributions in dynamical multiagent systems

In the evolutionary version of the minority game, agents update their strategies (gene-value $p$) in order to improve their performance. Motivated by recent intriguing results obtained for prize-to-fine ratios which are smaller than unity, we explore the system's dynamics with a strategy updating rule of the form $p \to p \pm \delta p$ ($0 \leq p \leq 1$). We find that the strategy distribution depends strongly on the values of the prize-to-fine ratio $R$, the length scale $\delta p$, and the type of boundary condition used. We show that these parameters determine the amplitude and frequency of the the temporal oscillations observed in the gene space. These regular oscillations are shown to be the main factor which determines the strategy distribution of the population. In addition, we find that agents characterized by $p={1 \over 2}$ (a coin-tossing strategy) have the best chances of survival at asymptotically long times, regardless of the value of $\delta p$ and the boundary conditions used.Comment: 4 pages, 7 figure

Relating the microscopic rules in coalescence-fragmentation models to the macroscopic cluster size distributions which emerge

Coalescence-fragmentation problems are of great interest across the physical, biological, and recently social sciences. They are typically studied from the perspective of the rate equations, at the heart of such models are the rules used for coalescence and fragmentation. Here we discuss how changes in these microscopic rules affect the macroscopic cluster-size distribution which emerges from the solution to the rate equation. More generally, our work elucidates the crucial role that the fragmentation rule can play in such dynamical grouping models. We focus on two well-known models whose fragmentation rules lie at opposite extremes setting the models within the broader context of binary coalescence-fragmentation models. Further, we provide a range of generalizations and new analytic results for a well-known model of social group formation [V. M. Eguiluz and M. G. Zimmermann, Phys. Rev. Lett. 85, 5659 (2000)]. We develop analytic perturbation treatment of the original model, and extend the mathematical to the treatment of growing and declining populations

Targeted treatments for fragile X syndrome

Fragile X syndrome (FXS) is the most common identifiable genetic cause of intellectual disability and autistic spectrum disorders (ASD), with up to 50% of males and some females with FXS meeting criteria for ASD. Autistic features are present in a very high percent of individuals with FXS, even those who do not meet full criteria for ASD. Recent major advances have been made in the understanding of the neurobiology and functions of FMRP, the FMR1 (fragile X mental retardation 1) gene product, which is absent or reduced in FXS, largely based on work in the fmr1 knockout mouse model. FXS has emerged as a disorder of synaptic plasticity associated with abnormalities of long-term depression and long-term potentiation and immature dendritic spine architecture, related to the dysregulation of dendritic translation typically activated by group I mGluR and other receptors. This work has led to efforts to develop treatments for FXS with neuroactive molecules targeted to the dysregulated translational pathway. These agents have been shown to rescue molecular, spine, and behavioral phenotypes in the FXS mouse model at multiple stages of development. Clinical trials are underway to translate findings in animal models of FXS to humans, raising complex issues about trial design and outcome measures to assess cognitive change that might be associated with treatment. Genes known to be causes of ASD interact with the translational pathway defective in FXS, and it has been hypothesized that there will be substantial overlap in molecular pathways and mechanisms of synaptic dysfunction between FXS and ASD. Therefore, targeted treatments developed for FXS may also target subgroups of ASD, and clinical trials in FXS may serve as a model for the development of clinical trial strategies for ASD and other cognitive disorders

Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities

Chronic obstructive pulmonary disease (COPD) and lung cancer are major lung diseases affecting millions worldwide. Both diseases have links to cigarette smoking and exert a considerable societal burden. People suffering from COPD are at higher risk of developing lung cancer than those without, and are more susceptible to poor outcomes after diagnosis and treatment. Lung cancer and COPD are closely associated, possibly sharing common traits such as an underlying genetic predisposition, epithelial and endothelial cell plasticity, dysfunctional inflammatory mechanisms including the deposition of excessive extracellular matrix, angiogenesis, susceptibility to DNA damage and cellular mutagenesis. In fact, COPD could be the driving factor for lung cancer, providing a conducive environment that propagates its evolution. In the early stages of smoking, body defences provide a combative immune/oxidative response and DNA repair mechanisms are likely to subdue these changes to a certain extent; however, in patients with COPD with lung cancer the consequences could be devastating, potentially contributing to slower postoperative recovery after lung resection and increased resistance to radiotherapy and chemotherapy. Vital to the development of new-targeted therapies is an in-depth understanding of various molecular mechanisms that are associated with both pathologies. In this comprehensive review, we provide a detailed overview of possible underlying factors that link COPD and lung cancer, and current therapeutic advances from both human and preclinical animal models that can effectively mitigate this unholy relationship